Impaired Central Chemoreceptor Function and Chronic Hypoventilation Many Years Following Poliomyelitis

Solliday, Norman H.; Gaensler, Edward A.; Schwaber, Jules R.; Parker, Thomas

doi:10.1159/000193108

Cited by 21 publications

(3 citation statements)

References 14 publications

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“…lt has been reported that some individuals with bulbar polio (P BM) have measurable dysfunction of respiratory control and irregular breathing during sleep [8,10). However, our group of bulbar polio survivors had nonnaJ respiratory mechanics with the exception of a slight reduction in expiratory muscle strength.…”

Section: Discussioncontrasting

confidence: 53%

Respiratory function during wakefulness and sleep among survivors of respiratory and non-respiratory poliomyelitis

Dolmage

Ma²,

Goldstein³

1992

Eur Respir J

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The purpose of this study was to determine whether there is a difference in respiratory mechanics and gas exchange between polio survivors and healthy, age-matched controls during wakefulness and sleep. Polio survivors were divided into four groups. The first group included those who had evidence of respiratory muscle involvement originally (PRM) and the second group included those who had bulbar muscle involvement originally (PBM). The third and fourth groups had only limb involvement originally but were separated by absence (PSL) or presence of a scoliosis (PSS) at the time of their evaluation. Each subject completed baseline and one year follow-up measurements of lung volumes, diffusion, flow rates, respiratory muscle strength, central and peripheral chemoreflexes and arterial blood gases. Sleep measurements included a full respiratory polysomnographic study. Fifty polio survivors and 13 controls completed the study. The PRM and PSS groups had an elevated arterial carbon dioxide tension (PaCO2) (mean +/- SE 6.0 +/- 0.4 and 6.0 +/- 0.3 kPa, respectively), reduced vital capacity (2.8 +/- 0.3 and 2.9 +/- 0.3 l, respectively), reduced maximal inspiratory pressure (-5.9 +/- 0.7 and -5.4 +/- 0.8 kPa, respectively) and reduced maximal expiratory pressure (9.8 +/- 1.1 and 9.1 +/- 1.2 kPa, respectively), when compared with non-polio controls. During sleep PRM and PSS groups experienced a higher PaCO2 (6.5 +/- 0.5 and 6.7 +/- 0.4 kPa, respectively) and a lower arterial oxygen saturation (SaO2) (89 +/- 4 and 86 +/- 3%, respectively). There were no differences among groups for diffusion, flow rates and chemoreflexes. All other polio survivors showed essentially normal respiratory function.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussioncontrasting

confidence: 53%

Respiratory function during wakefulness and sleep among survivors of respiratory and non-respiratory poliomyelitis

Dolmage

Ma²,

Goldstein³

1992

Eur Respir J

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“…In some, but not all of the cases there is a history of a previous neurological disorder such as encephalitis, meningitis, Parkinsonism or poliomyelitis. Twenty-two separate case reports in which exercise was studied have been reviewed by Solliday, Gaensler, Schwaber & Parker (1974). All cases were hypercapnic and hypoxic when at rest; upon mild exercise, seven had no change in blood gases, five improved and ten had worsening blood gases.…”

Section: Previous Exercise Studies In Adults With Alveolar Hypoventilmentioning

confidence: 99%

Ventilatory responses to exercise in humans lacking ventilatory chemosensitivity.

Shea

Andrés

Shannon

et al. 1993

The Journal of Physiology

119

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SUMMARY1. In healthy humans during aerobic exercise ventilation increases and mean arterial Pco2 usually remains constant over a wide range of CO2 production. years) with abnormally low ventilatory responses to steady-state increased endtidal PCO2 ( <9 ml min-' kg-' mmHg-') and five age-matched controls.4. Depth and rate of breathing, end-tidal Pco,, end-tidal P02, CO2 production, 02 utilization and heart rate were monitored during the following conditions: whilst subjects stood at rest; following the onset of treadmill exercise (4 m.p.h.); during steady-state exercise (4 m.p.h.); during an incremental maximal exercise test; and during recovery from exercise. 5. There were no significant differences in the ventilatory responses between CCHS subjects and controls during the onset of treadmill exercise, in the dynamic response in achieving the steady-state exercise, during steady-state exercise, in the recovery from steady-state exercise, or during incremental exercise (up to the point of presumed blood lactate accumulation, as indicated by gas exchange criteria).There was a very small mean increase in PCO2 in both groups during steady-state exercise (controls 1'4 mmHg; CCHS 2-2 mmHg).6. The only differences which emerged between groups were (i) slightly more variability in PCO2 in the CCHS group during steady-state exercise, and (ii) the CCHS subjects did not hyperventilate, as the controls did, at exercise levels above the point of presumed blood lactate accumulation. 7. Breath-by-breath coefficient of variation of ventilation was significantly reduced in both groups during steady-state exercise compared to rest. There were MS 1714 S. A. SHEA AND OTHERS no differences between groups in either state.8. We conclude that chemoreceptors are not necessary for an appropriate ventilatory response to aerobic exercise. Hence, other stimuli, such as afferent information from the exercising limbs or signals related to activation of the motor cortex, can increase alveolar ventilation in close proportion to C02 production.9. The lack of hyperventilatory response to blood lactate accumulation during heavy exercise provides good evidence that these CCHS patients have ineffective peripheral chemoreception.

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“…The goal again was to prevent hypoxemia and hypercarbia during the hours of rest. [23][24][25] Two patients in Group V required total support of mechanical ventilation. However, the goal in two patients with diaphragmatic paralysis was providing rest for the accessory muscles of respiration at night and preventing severe hypoxemia, particularly during REM sleep.…”

Section: Discussionmentioning

confidence: 99%

Clinical considerations in the implementation of home care ventilation: observations in 24 patients

et al. 1983

Cleveland Clinic Journal of Medicine

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The assessment and management of 24 patients with compromized respiratory systems, in our experience, suggest that the physiological support delivered by mechanical ventilation can improve the clinical status of such patients. Clinical observations of recurrent respiratory failure, progressive deterioration in exercise tolerance, and/or symptoms of alveolar hypoventilation due to hypercarbia and hypoxemia were sufficient to warrant clinical trials of assisted mechanical ventilation. Long-term management goals included supportive care for patients with progressive neuromuscular diseases and rehabilitation in patients with restrictive chest wall disease or diaphragmatic paralysis.

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Impaired Central Chemoreceptor Function and Chronic Hypoventilation Many Years Following Poliomyelitis

Cited by 21 publications

References 14 publications

Respiratory function during wakefulness and sleep among survivors of respiratory and non-respiratory poliomyelitis

Respiratory function during wakefulness and sleep among survivors of respiratory and non-respiratory poliomyelitis

Ventilatory responses to exercise in humans lacking ventilatory chemosensitivity.

Clinical considerations in the implementation of home care ventilation: observations in 24 patients

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